Differential bronchial and pulmonary vascular responses to vagal stimulation in the pig.

The pulmonary and bronchial vascular responses and changes in bronchial tone upon vagal stimulation (240 impulses at 2 Hz or 10 Hz) were studied in anaesthetized pigs paralyzed with pancuronium. The acetylcholine-evoked vasodilatation in the tracheobronchial circulation had the same magnitude when using pancuronium or succinylcholine as skeletal muscle relaxants. Atropine-sensitive bradycardia, hypotension and bronchoconstriction were observed upon vagal stimulation. A vasoconstrictor response in the pulmonary vascular bed and clear-cut vasodilatation in the bronchial circulation supplied by the bronchial artery also occurred upon vagal stimulation. The vagally-evoked increase in pulmonary vascular resistance was markedly reduced after atropine while the bronchial vasodilatation was unchanged. This suggests that the vagally-induced increase in bronchial blood flow was not secondary to changes in the pulmonary circulation. Furthermore, the pulmonary vasoconstrictor response caused by vagal stimulation under control conditions is probably explained by reflex sympathetic activation due to the fall in systemic blood pressure. These data indicate selective vagal non-cholinergic influence of blood flow in the bronchial vascular bed compared to the pulmonary circulation.     

Responses of the bronchial and pulmonary circulations to short‐term nitric oxide inhalation before and after endotoxaemia in the pig

The physiological responses of the bronchial circulation to acute lung injury and endotoxin shock are largely unexplored territory. This study was carried out to study the responsiveness of the bronchial circulation to nitric oxide (NO) inhalation before and after endotoxaemia, in comparison with the pulmonary circulation, as well as to study changes in bronchial blood flow during endotoxaemia. Six anaesthetized pigs (pre‐treated with the cortisol‐synthesis inhibitor metyrapone) received an infusion of 10 µg/kg endotoxin during 2 h. Absolute bronchial blood flow was measured via an ultrasonic flow probe around the bronchial artery. The pigs received increasing doses of inhaled NO over 5 min each (0, 0.2, 2 and 20 ppm) before and after 4 h of endotoxaemia. The increase in bronchial vascular conductance during 5 min of inhalation of 20 ppm NO before endotoxin shock was significantly higher (area under curve (AUC) 474.2 ± 84.5% change) than after endotoxin shock (AUC 118.2 ± 40.4%, P < 0.05 Mann–Whitney U‐test). The reduction of the pulmonary arterial pressure by 20 ppm NO was not different. A short rebound effect of the pulmonary arterial pressure occurred after discontinuation of inhaled NO before endotoxaemia (AUC values above baseline 54.4 ± 19.7% change), and was virtually abolished after endotoxaemia (AUC 6.1 ± 4.0%, P = 0.052, Mann–Whitney U‐test). Our results indicate that the responsiveness of the bronchial circulation to inhalation of increasing doses of inhaled NO during endotoxin shock clearly differ from the responsiveness of the pulmonary circulation. The reduced responsiveness of the bronchial circulation is probably related to decreased driving pressure for the bronchial blood flow. The absence of the short rebound effect on pulmonary arterial pressure (PAP) after induction of shock could be related to maximum constriction of the pulmonary vessels at 4 h.     

Cardiac vagal and sympathetic nerve responses to baroreceptor stimulation in the dog

The effects of ascending stepwise pressure changes in the isolated carotid sinuses on cardiac vagal and sympathetic nerve activities were studied in anesthetized, open chest dogs. The steady state responses of the cardiac vagal and the sympathetic nerve activity and arterial blood pressure were plotted against the sinus pressure and the relations were approximated by the normal distribution function (response curve). The sinus pressure- vs. reflex gain relations (reflex gain curve) were approximated by the normal density function. The maximum gain and the range of change were found to be greater for the vagal than for the sympathetic and arterial pressure responses. The sinus pressure values derived from response curves and reflex gain curves for vagal and sympathetic nerve responses were close to each other, while these values and those obtained from arterial pressure responses were considerably apart. It was concluded that: (1) The cardiac vagal neurons are more sensitive to the baroreceptor input than the sympathetic neurons; (2) The similar type of baroreceptor afferent inputs reach the cardiac vagal and the sympathetic structures which are controlling the autonomic outflows.     

Nervous control of pancreatic endocrine secretion in pigs IV. The effect of somatostatin on the insulin and glucagon responses to electrical vagal stimulation and to intraarterial acetylcholine

We studied the effect of a primed i.v. infusion of somatostatin (0.5 μg×min^–1×kg^–1 on the glucose dependent insulin and glucagon responses to electrical stimulation of the vagus nerves or to i.a. acetylcholine in anesthetized pigs. Somatostatin completely abolished the insulin and glucagon responses to ongoing vagal stimulation; after 70 min somatostatin infusion the response to reiterated stimulation was profoundly inhibited. After termination of the somatostatin infusion, a considerable rebound secretion of insulin and glucagon was noted. By contrast, the endocrine response to acetylcholine persisted in spite of the somatostatin administration. Blood glucose increased slightly during somatostatin infusion. The results suggest that somatostatin inhibits the responses to vagal stimulation by interference with the neural transmission to the pancreatic islets rather than by inhibition of the islet cells themselves; acetylcholine may be involved in this neural transmission (acting on nicotinic receptors.     

迷走神经刺激对缺血性心肌损伤保护作用的研究进展

缺血性心肌病是高病死率的常见疾病.研究表明,自主神经系统的功能与缺血性心肌病的发病及预后密切相关.在心肌缺血发生前后,给予迷走神经刺激能够显著减轻缺血造成的心肌损伤.本文重点讨论迷走神经刺激在缺血性心肌损伤方面的保护机制及其最新研究成果.     

Topographic anatomy of bronchial arteries in the pig: a corrosion cast study

The anatomy of porcine bronchial circulation has not been fully described. The purpose of this study was to investigate the extrapulmonary topographic anatomy of bronchial arteries in pig. Ten pigs weighing 15-25 kg were studied. Between one and four bronchial arteries were found in each pig. The bronchoesophageal artery (BEA), tracheobronchial artery (TBA), inferior bronchial artery (IBA) and accessory bronchial artery (ABA) were present in 10/10, 8/10, 6/10 and 2/10 animals, respectively. The trunk of BEA had a diameter of about 3 mm, a length of 1-7 mm, and originated from the anterior and medial aspect of the descending thoracic aorta at the level between the 2nd and 4th thoracic vertebrae (T2-T4) in all animals. The extrapulmonary topographic anatomy of bronchial arteries in pigs exhibits similarities to that of humans. BEA is the main blood supplier of the porcine tracheobronchial tree with a relatively constant location of origin and a sufficient size for anastomosis. These characteristics render BEA the ideal vessel for bronchial revascularization in pigs.     

Differential plasma corticosterone responses to hippocampal stimulation

Summary The effect of limbic forebrain stimulation on pituitary-adrenal function was assessed by evaluating plasma corticosterone obtained prior to and following sham or electrical stimulation of urethane (1.20 g/kg) anesthetized female rats. Cortical electroencephalogram (EEG), electrocardiogram (ECG), heart rate (HR), mean arterial blood pressure (MAP), and respiration were routinely monitored. Timed blood samples (0.25 ml) were obtained from a catherized femoral artery. The HR (Bts/min), MAP (mm of Hg), and corticosterone levels (g/dl) for 7 non-stimulated rats averaged over 6 sampling periods were 385±19, 95±6, and 70.3±5.8 respectively. In electrically or sham stimulated rats, blood samples were taken just prior to stimulation (biphasic square waves, 100 A, 50 or 60 Hz, 1 ms, 1 s on/1 s off for 15 or 30 min) and 5, 10, 15, and 30 min after initiation of stimulation.Significant changes in plasma corticosterone levels were obtained following stimulation of hippocampal and amygdaloid areas. In contrast, no change in corticosterone concentration was observed following stimulation of cortex, corpus callosum, fornix and a variety of other CNS areas. Detailed analysis of hippocampal influence on urethane stimulated plasma corticosterone levels showed increased plasma corticosterone levels following stimulation of CA1. In contrast, stimulation of CA3, dentate (includes CA4) and the subiculum produced significant decreases in plasma corticosterone levels. No change in corticosterone levels was observed following sham stimulation. Collectively, these data indicate that consideration must be given to the possibility that differential neuroendocrine regulatory mechanisms reside within various limbic forebrain complexes and that electrical stimulation of limbic forebrain sites of urethane anesthetized rats may provide information regarding sites inhibitory to pituitary-adrenal activity.     

The effect of propranolol on the serotonin concentration in the portal plasma after vagal nerve stimulation in the cat

Efferent cervical vagal nerve stimulation in the cat caused a marked increase of the portal plasma 5-HT concentration. This increase was more than two-fold within 15 min of stimulation. After cessation of stimulation portal plasma 5-HT returned to basal levels within 10 min. Treatment with the β-adrenoceptor antagonist propranolol, in various doses (0.1–2 mg/kg b.wt.), did not abolish but significantly reduced the response to vagal stimulation, particularly during the final part of the stimulation period. The results confirm the existence of a β-adrenoceptor-mediated release of 5-HT, but also suggest that other mechanisms for 5-HT release may be involved in the response on vagal nerve stimulation.     

Oral lesions in the chicken: Behavioural responses following nociceptive stimulation

The behaviour of normal birds and birds with ulcerated buccal lesions was described following oral stimulation with Acetylcholine chloride (ACh) and Bradykinin (BK). Both groups of birds showed normal oral behaviour but a number of birds with oral lesions showed a behaviour pattern which had been previously seen in our laboratory following nociceptive stimulation. The birds remained motionless in a crouch-like stance with the head pulled into the body and a significantly reduced number of alert head movements. The onset and duration of this immobility response was compared with reports of pain in humans in the blister-base test using similar concentrations of ACh and BK. It was concluded that nocifensive responses of the chicken fulfil many of the requirements for the definition of pain in animals.     

Differential chronotropic and dromotropic responses to focal stimulation of cardiac vagal ganglia in the rat

Vagal cardioinhibition is exerted through a reduction not only in the heart rate but also in the rate of propagation of the cardiac action potential and in myocardial contractility. In several species, such effects can be produced independently by selective activation of ganglia in identified 'fat pads'. In this study we investigate differential control of heart rate and atrioventricular conduction by two ganglionic clusters in the rat, a species increasingly important in studies of cardiovascular control. Epicardial sites producing low-threshold changes in P-P and P-R interval of the ECG in an arterially perfused preparation were explored with concentric bipolar stimulating electrodes. Stimulation sites centred on two principal ganglia, the sinoatrial (SA) ganglion at the junction of the right superior vena cava and right atrium, and the atrioventricular (AV) ganglion at the junction of the inferior pulmonary veins and left atrium. Stimulation of the SA ganglion decreased heart rate in all preparations, with little or no effect on AV conduction in one-third. Stimulation of the AV ganglion consistently slowed conduction without eliciting a comparable bradycardia. Responses survived blockade of ganglionic transmission by trimetaphan, with an enhanced chronotropic selectivity to SA ganglion stimulation, suggesting that co-excitation of preganglionic elements en passant may have contributed to the earlier mixed responses. Effective stimulation sites were precisely circumscribed and corresponded to principal ganglionic clusters confirmed histologically. We conclude that cardiac vagal ganglia in the rat show a topographical functional organisation and are amenable to investigation using the arterially perfused preparation.     

Bilateral reflex effects on phrenic nerve activity in response to single-shock vagal stimulation

The bilateral reflex actions of vagus nerve afferent signals on phrenic efferent activity have been tested by unilateral graded single shock electrical stimulation. An early excitation (latency 3–5 msec) was more prominent in the phrenic nerve contralateral to the stimulated vagus. Spinal cord hemisection at C₃ eliminated both contralateral and ipsilateral responses: thus, both were mediated via descending tracts in the contralateral cord. A bilaterally symmetrical early inhibition (latency 8–12 msec) followed the early excitation. The electrical thresholds for evoking the early responses and the temperature for blocking these responses during graded vagal cooling were closely similar to the threshold and blocking temperature for pulmonary stretch receptor afferents. Higher stimulus strengths evoked a strong, bilaterally similar, late excitation (latency 12–20 msec) followed by a late inhibition. At very high stimulus strengths a third excitation (latency 25–30 msec) could appear. Sometimes these responses were followed by lowered phrenic activity for the remainder of inspiration. Single shock stimulation of the intact vagus nerve or of the peripheral end of the cut recurrent laryngeal nerve provoked. by the contraction of laryngeal muscles, a strong, short latency (12 msec) inhibition of phrenic activity mediated by superior laryngeal nerve afferents. The implications of these results with respect to the reflex pathways of the different responses and their possible integration in the central respiratory control mechanisms are discussed.     

Specific adrenergic responses of smooth muscles in the vascular wall of guinea pig pulmonary arteries during ovalbumin sensitization

The adrenergic contractile responses of smooth muscles in the vascular wall of guinea pig pulmonary arteries were studied during ovalbumin sensitization. Sensitization was followed by inhibition of contractile responses to an α-adrenoceptor agonist mesatone, prevented endothelium-derived relaxation, and potentiated the contractile response to isoproterenol. Administration of a β-adrenoceptor agonist isoproterenol potentiated the increase in mechanical strain of smooth muscles in the pulmonary artery precontracted with high-potassium Krebs solution. Removal of the endothelium had no effect on the contractile response of smooth muscle segments from the pulmonary artery of intact and sensitized guinea pigs to β-adrenergic influences. The contractile responses of smooth muscles of the pulmonary artery are associated with activity of the cAMP-dependent signal system and play a role in the pathogenesis of ventilation-perfusion disturbances during atopic inflammation. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 145, No. 6, pp. 617–620, June, 2008     

Mothers' responses to children's negative emotions and child emotion regulation: the moderating role of vagal suppression

The current study examined the moderating effect of children's cardiac vagal suppression on the association between maternal socialization of negative emotions (supportive and nonsupportive responses) and children's emotion regulation behaviors. One hundred and ninety-seven 4-year-olds and their mothers participated. Mothers reported on their reactions to children's negative emotions and children's regulatory behaviors. Observed distraction, an adaptive self-regulatory strategy, and vagal suppression were assessed during a laboratory task designed to elicit frustration. Results indicated that children's vagal suppression moderated the association between mothers' nonsupportive emotion socialization and children's emotion regulation behaviors such that nonsupportive reactions to negative emotions predicted lower observed distraction and lower reported emotion regulation behaviors when children displayed lower levels of vagal suppression. No interaction was found between supportive maternal emotion socialization and vagal suppression for children's emotion regulation behaviors. Results suggest physiological regulation may serve as a buffer against nonsupportive emotion socialization.